Autoantibodies and Rheumatologic Manifestations in Hepatitis C Virus Infection

SIMPLE SUMMARY: In patients with HCV, rheumatic manifestations are mostly mediated by immunological mechanisms, rather than being related to the viral infection of extrahepatic tissues. Molecular mimicry of viral antigens, chronic stimulation of B cells and a bystander effect are some of the mechanisms for the development of autoimmune phenomena and lymphoproliferative disorders; these conditions can either be clinical, merely serological or both. Among these patients, the occurrence of auto-antibodies is a finding strictly associated with a chronic infectious trigger since HCV has been proved to induce a B-mediated response shortly after the activation of the innate immune system. Given this scenario, a rheumatic disorder can be found as it might coexist with the HCV infection thus giving an overlap syndrome in some patients. Nevertheless, direct-acting antiviral therapies have largely demonstrated to reduce the damage stemming from both systemic inflammatory phenomena and a persistent immune activation by promoting an early viral eradication. ABSTRACT: HCV is a virus that can cause chronic infection which can result in a systemic disease that may include many rheumatologic manifestations such as arthritis, myalgia, sicca syndrome, cryoglobulinemia vasculitis as well as other non-rheumatological disorders (renal failure, onco-haematological malignancies). In this population, the high frequency of rheumatoid factor (45–70%), antinuclear (10–40%) and anticardiolipin (15–20%) antibodies is a B-cell mediated finding sustained by the infection. However, the possibility that a primitive rheumatic pathology may coexist with the HCV infection is not to be excluded thus complicating a differential diagnosis between primitive and HCV-related disorders.